BackgroundAcute exacerbation of COPD (AECOPD) is associated with an increased hospitalization and mortality. Azithromycin and erythromycin are the recommended drugs to reduce the risk of exacerbations. However, the most suitable duration of therapy and drug-related adverse events are still a matter of debate. The aim of this meta-analysis was to assess the current evidence regarding the efficacy and safety of long-term macrolide treatment for COPD.Materials and methodsWe comprehensively searched PubMed, Embase, the Cochrane Library, and the Web of Science and performed a systematic review and cumulative meta-analysis of all randomized controlled trials (RCTs) and retrospective studies.ResultsEleven RCTs and one retrospective study including a total of 2,151 cases were carried out. Long-term macrolide treatment significantly reduced the total number of cases with one or more exacerbations (OR=0.40; 95% CI=0.24–0.65; P<0.01) and the rate of exacerbations per patient per year (risk ratio [RR]=0.60; 95% CI=0.45–0.78; P<0.01). Subgroup analyses showed that the minimum duration for drug efficacy for both azithromycin and erythromycin therapy was 6 months. In addition, macrolide therapy could improve the St George Respiratory Questionnaire (SGRQ) total score (P<0.01) but did not achieve the level of clinical significance. The frequency of hospitalizations was not significantly different between the treatment and control groups (P=0.50). Moreover, chronic azithromycin treatment was more likely to increase adverse events (P<0.01).ConclusionProphylactic azithromycin or erythromycin treatment has a significant effect in reducing the frequency of AECOPD in a time-dependent manner. However, long-term macrolide treatment could increase the occurrence of adverse events and macrolide resistance. Future large-scale, well-designed RCTs with extensive follow-up are required to identify patients in whom the benefits outweigh risks.

Background: Asthma is one of the most common chronic respiratory diseases in children. CD4+T cell plays a key role in the immune response which affects the pathogenesis of asthma. Genetic level of CD4+T cells on childhood allergic asthma remains unclear. In our study, we aimed to identify potential different expressed genes (DEGs) and pathways related to childhood allergic asthma by performing bioinformatics analysis of dataset.Methods: GSE40887 dataset from Gene Expression Omnibus (GEO) was used for bioinformatics analysis. Limma package in R was used to detect DEGs. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were carried by Database for Annotation, Visualization and Integrated Discovery (DAVID). The construction of protein-protein interaction (PPI) network of the DEGs was performed by Search Tool for the Retrieval of Interacting Genes (STRING) and Cytoscape. Hub genes were identified through cytoHubba in Cytoscape. Results: In all, 200 up-regulated genes and 69 down-regulated genes were identified. Up-regulated genes were mainly enriched in: protein self-association, cellular response to hydrogen peroxide, plasma membrane. As for down-regulated genes, enzyme binding and detection of chemical stimulus involved in sensory perception of smell, nucleolus were enriched. Only one KEGG pathway was enriched: olfactory transduction. In addition, top 10 hub genes were found including: PRPF19, CCAR1, CWC15, PRPF38A, PRCC, KRR1, RPS3, PDCD11, MKI67, and NUF2. Conclusion: Several DEGs (SNORD46, RPS3, OR5E1P, OR56A5 and OR51B6, and PDCD11), one pathway (olfactory transduction) and one biological process (cellular response to hydrogen peroxide) were found might associate to childhood allergic asthma. Our results may provide inspiration for other researchers on DEGs and pathways in CD4+T cells of childhood allergic asthma.